Home GPCR & G Protein Glucagon Receptor chemical Albiglutide Fragment

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Albiglutide Fragment Glucagon Receptor chemical

Cat.No.S3734

Albiglutide fragment is one copy of a 30-amino-acid sequence of modified human GLP-1 (fragment 7-36).
Albiglutide Fragment Glucagon Receptor chemical Chemical Structure

Chemical Structure

Molecular Weight: 3283.6

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Quality Control

Batch: Purity: 99.71%
99.71

Solubility

In vitro
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Water : 100 mg/mL

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Chemical Information, Storage & Stability

Molecular Weight 3283.6 Formula

C148H224N40O45

 Storage (From the date of receipt)
CAS No. 782500-75-8 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles CCC(C)C(C(=O)NC(C)C(=O)NC(CC1=CNC2=CC=CC=C21)C(=O)NC(CC(C)C)C(=O)NC(C(C)C)C(=O)NC(CCCCN)C(=O)NCC(=O)NC(CCCNC(=N)N)C(=O)N)NC(=O)C(CC3=CC=CC=C3)NC(=O)C(CCC(=O)O)NC(=O)C(CCCCN)NC(=O)C(C)NC(=O)C(C)NC(=O)C(CCC(=O)N)NC(=O)CNC(=O)C(CCC(=O)O)NC(=O)C(CC(C)C)NC(=O)C(CC4=CC=C(C=C4)O)NC(=O)C(CO)NC(=O)C(CO)NC(=O)C(C(C)C)NC(=O)C(CC(=O)O)NC(=O)C(CO)NC(=O)C(C(C)O)NC(=O)C(CC5=CC=CC=C5)NC(=O)C(C(C)O)NC(=O)CNC(=O)C(CCC(=O)O)NC(=O)CNC(=O)C(CC6=CN=CN6)N

Mechanism of Action

In vitro

Albiglutide is a recombinant fusion protein consisting of two copies of a 30-amino-acid sequence of modified human GLP-1 (fragment 7-36), modified with a glycine substituted for the naturally occurring alanine at position 8 in order to augment resistance to DPP-4.
In vivo

Glucose lowering occurs within 24 h after a single dose of albiglutide, as a result of binding of the molecule to the GLP-1 receptor. The reduction in both fasting and postprandial glucose levels is dose related. Albiglutide is less potent than GLP-1. In animal models of diabetes, albiglutide administration stimulates increased β-cell mass. Following SC administration of a single 30-mg dose to patients with type 2 diabetes, maximum concentration is reached in 3-5 days with half-life of 3.6-6.8 days. The apparent volume of distribution after a single dose of albiglutide was 8.2-18.5 L. The eventual fate of albiglutide in the circulation is degradation into small peptides and individual amino acids. Albiglutide had no apparent effects on cardiovascular function, heart rate, electrocardiographic intervals, or respiratory function and did not produce any evidence of electrocardiographic abnormalities or arrhythmias in male cynomolgus monkeys. Furthermore, there were no albiglutide-related effects on neurobehavioral functional assessments. Albiglutide does not cross the blood–brain barrier to reach the satiety centers. Albiglutide reduced myocardial infarct size and improved cardiac function and energetics following myocardial I/R injury which are associated with enhanced myocardial glucose uptake and a shift toward a more energetically favorable substrate metabolism by increasing both glucose and lactate oxidation.
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